Polarization and reprogramming of myeloid-derived suppressor cells
Myeloid-derived suppressor cells (MDSC) have recently emerged as one of the central regulators of the immune system. In recent years, interest in understanding MDSC biology and applying MDSC for therapeutic purpose has exploded exponentially. Despite recent progress in MDSC biology, the mechanisms u...
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Veröffentlicht in: | Journal of molecular cell biology 2013-06, Vol.5 (3), p.207-209 |
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creator | Yang, Wen-Chin Ma, Ge Chen, Shu-Hsia Pan, Ping-Ying |
description | Myeloid-derived suppressor cells (MDSC) have recently emerged as one of the central regulators of the immune system. In recent years, interest in understanding MDSC biology and applying MDSC for therapeutic purpose has exploded exponentially. Despite recent progress in MDSC biology, the mechanisms underlying MDSC development from expansion and activation to polarization in different diseases remain poorly understood. More recent studies have demonstrated that two MDSC subsets, M (monocytic)-MDSC and G (granulocytic)-MDSC, are able to polarize from a classically activated phenotype (M1) to an alternatively activated one (M2), or vice versa, in tumor-bearing mice. This phenotypic polarization affects MDSC function and disease progression. In this article, we summarize and discuss polarization, mechanism and therapeutic potential of MDSC. An emphasis is placed on the emerging concept of reprogramming MDSC polarization as a therapeutic strategy. |
doi_str_mv | 10.1093/jmcb/mjt009 |
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In recent years, interest in understanding MDSC biology and applying MDSC for therapeutic purpose has exploded exponentially. Despite recent progress in MDSC biology, the mechanisms underlying MDSC development from expansion and activation to polarization in different diseases remain poorly understood. More recent studies have demonstrated that two MDSC subsets, M (monocytic)-MDSC and G (granulocytic)-MDSC, are able to polarize from a classically activated phenotype (M1) to an alternatively activated one (M2), or vice versa, in tumor-bearing mice. This phenotypic polarization affects MDSC function and disease progression. In this article, we summarize and discuss polarization, mechanism and therapeutic potential of MDSC. An emphasis is placed on the emerging concept of reprogramming MDSC polarization as a therapeutic strategy.</description><identifier>ISSN: 1674-2788</identifier><identifier>EISSN: 1759-4685</identifier><identifier>DOI: 10.1093/jmcb/mjt009</identifier><identifier>PMID: 23532593</identifier><language>eng</language><publisher>United States: Oxford University Press</publisher><subject>Animals ; Cell Line, Tumor ; Cell Polarity ; Granulocytes - immunology ; Mice ; Monocytes - immunology ; Myeloid Cells - immunology ; Neoplasms - immunology ; Neoplasms - metabolism ; Neoplasms - pathology ; Phenotype</subject><ispartof>Journal of molecular cell biology, 2013-06, Vol.5 (3), p.207-209</ispartof><rights>The Author (2013). Published by Oxford University Press on behalf of , IBCB, SIBS, CAS. 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In recent years, interest in understanding MDSC biology and applying MDSC for therapeutic purpose has exploded exponentially. Despite recent progress in MDSC biology, the mechanisms underlying MDSC development from expansion and activation to polarization in different diseases remain poorly understood. More recent studies have demonstrated that two MDSC subsets, M (monocytic)-MDSC and G (granulocytic)-MDSC, are able to polarize from a classically activated phenotype (M1) to an alternatively activated one (M2), or vice versa, in tumor-bearing mice. This phenotypic polarization affects MDSC function and disease progression. In this article, we summarize and discuss polarization, mechanism and therapeutic potential of MDSC. An emphasis is placed on the emerging concept of reprogramming MDSC polarization as a therapeutic strategy.</description><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Cell Polarity</subject><subject>Granulocytes - immunology</subject><subject>Mice</subject><subject>Monocytes - immunology</subject><subject>Myeloid Cells - immunology</subject><subject>Neoplasms - immunology</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - pathology</subject><subject>Phenotype</subject><issn>1674-2788</issn><issn>1759-4685</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkM9LwzAUx4MobsydvEuPglSTJmnSi6DDXzDQg55DkiYzo2lq0g3mX2_H5tBcXuB9-L73PgCcI3iNYIVvll6rG7_sIayOwBgxWuWk5PR4-JeM5AXjfASmKS3h8DDHmMNTMCowxQWt8Bjcv4VGRvctexfaTLZ1Fk0XwyJK7127yILN_MY0wdV5baJbmzpLq66LJqUQM22aJp2BEyubZKb7OgEfjw_vs-d8_vr0Mrub55oQ1ucEcQaZhUpZiCyqubKSVFRSXSkjYUm14lZjzTRC0haF4YhhRTHTpLRQF3gCbne53Up5U2vT9lE2oovOy7gRQTrxv9O6T7EIa4HLipaUDQGX-4AYvlYm9cK7tD1BtiaskkCDFcI4LPmAXu1QHUNK0djDGATFVrzYihc78QN98XezA_urGf8AvKWCOg</recordid><startdate>20130601</startdate><enddate>20130601</enddate><creator>Yang, Wen-Chin</creator><creator>Ma, Ge</creator><creator>Chen, Shu-Hsia</creator><creator>Pan, Ping-Ying</creator><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130601</creationdate><title>Polarization and reprogramming of myeloid-derived suppressor cells</title><author>Yang, Wen-Chin ; Ma, Ge ; Chen, Shu-Hsia ; Pan, Ping-Ying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c447t-418707f0bbf01f1d8bfa495a5c9bea065cb8fc3c7c11af22e8173b537c46f0c23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Cell Polarity</topic><topic>Granulocytes - immunology</topic><topic>Mice</topic><topic>Monocytes - immunology</topic><topic>Myeloid Cells - immunology</topic><topic>Neoplasms - immunology</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - pathology</topic><topic>Phenotype</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yang, Wen-Chin</creatorcontrib><creatorcontrib>Ma, Ge</creatorcontrib><creatorcontrib>Chen, Shu-Hsia</creatorcontrib><creatorcontrib>Pan, Ping-Ying</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of molecular cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yang, Wen-Chin</au><au>Ma, Ge</au><au>Chen, Shu-Hsia</au><au>Pan, Ping-Ying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Polarization and reprogramming of myeloid-derived suppressor cells</atitle><jtitle>Journal of molecular cell biology</jtitle><addtitle>J Mol Cell Biol</addtitle><date>2013-06-01</date><risdate>2013</risdate><volume>5</volume><issue>3</issue><spage>207</spage><epage>209</epage><pages>207-209</pages><issn>1674-2788</issn><eissn>1759-4685</eissn><abstract>Myeloid-derived suppressor cells (MDSC) have recently emerged as one of the central regulators of the immune system. In recent years, interest in understanding MDSC biology and applying MDSC for therapeutic purpose has exploded exponentially. Despite recent progress in MDSC biology, the mechanisms underlying MDSC development from expansion and activation to polarization in different diseases remain poorly understood. More recent studies have demonstrated that two MDSC subsets, M (monocytic)-MDSC and G (granulocytic)-MDSC, are able to polarize from a classically activated phenotype (M1) to an alternatively activated one (M2), or vice versa, in tumor-bearing mice. This phenotypic polarization affects MDSC function and disease progression. In this article, we summarize and discuss polarization, mechanism and therapeutic potential of MDSC. An emphasis is placed on the emerging concept of reprogramming MDSC polarization as a therapeutic strategy.</abstract><cop>United States</cop><pub>Oxford University Press</pub><pmid>23532593</pmid><doi>10.1093/jmcb/mjt009</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cell Line, Tumor Cell Polarity Granulocytes - immunology Mice Monocytes - immunology Myeloid Cells - immunology Neoplasms - immunology Neoplasms - metabolism Neoplasms - pathology Phenotype |
title | Polarization and reprogramming of myeloid-derived suppressor cells |
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